The occurrence of dyslipidaemia, which is an established risk factor for cardiovascular diseases, has been attributed to multiple factors including genetic and environmental factors. We used a genetic risk score (GRS) to assess the interactions between genetic variants and dietary factors on lipid-related traits in a cross-sectional study of 190 Brazilians (mean age: 21 ± 2 years). Dietary intake was assessed by a trained nutritionist using three 24-h dietary recalls. The high GRS was significantly associated with increased concentration of TAG (beta = 0·10 mg/dl, 95 % CI 0·05–0·16; P < 0·001), LDL-cholesterol (beta = 0·07 mg/dl, 95 % CI 0·04, 0·11; P < 0·0001), total cholesterol (beta = 0·05 mg/dl, 95 % CI: 0·03, 0·07; P < 0·0001) and the ratio of TAG to HDL-cholesterol (beta = 0·09 mg/dl, 95 % CI: 0·03, 0·15; P = 0·002). Significant interactions were found between the high GRS and total fat intake on TAG:HDL-cholesterol ratio (Pinteraction = 0·03) and between the high GRS and SFA intake on TAG:HDL-cholesterol ratio (Pinteraction = 0·03). A high intake of total fat (>31·5 % of energy) and SFA (>8·6 % of energy) was associated with higher TAG:HDL-cholesterol ratio in individuals with the high GRS (beta = 0·14, 95 % CI: 0·06, 0·23; P < 0·001 for total fat intake; beta = 0·13, 95 % CI: 0·05, 0·22; P = 0·003 for SFA intake). Our study provides evidence that the genetic risk of high TAG:HDL-cholesterol ratio might be modulated by dietary fat intake in Brazilians, and these individuals might benefit from limiting their intake of total fat and SFA.

The present study was conducted to determine the effects of dietary terrestrial oils (TO) supplemented with l-carnitine on growth performance, biochemical and antioxidant response, lipid metabolism and inflammation in large yellow croaker (Larimichthys crocea). Three iso-nitrogenous and iso-lipidic experimental diets were formulated with FO (fish oil, the control group), 75 % TO (75 % FO was substituted by the oil mixture with equal amounts of soyabean oil, linseed oil and pork lard) and 75 % TOC (75 % TO supplemented with 800 mg/kg l-carnitine). Compared with the control group, feed efficiency ratio and specific growth rate were significantly increased in fish fed diets with 75 % TO and 75 % TOC. Hepatic lipid content, serum TAG level, LDL-cholesterol level and the mRNA expression of pro-inflammatory genes (tnfα and ifnγ) were significantly increased in fish fed the diet with 75 % TO compared with the control group. However, the supplementation of 800 mg/kg l-carnitine in the 75 % TO diet repressed hepatic lipid content, serum LDL-cholesterol level and the mRNA expression of tnfα and ifnγ in fish compared with fish fed the diet with 75 % TO. Total antioxidant capacity, the activity of superoxide dismutase, the mRNA expression of cpt-I and the activity of CPT-I were significantly increased in fish fed the diet with 75 % TOC compared with 75 % TO. In conclusion, these results suggested that the supplementation of 800 mg/kg l-carnitine in the diet with TO mixture could increase growth, antioxidant capacity and fatty acid oxidation and decrease the expression of inflammatory genes in large yellow croaker.

The objective of the present study was to investigate the effect of curcumin on insulin resistance (IR) and hepatic lipid accumulation in intra-uterine growth restriction (IUGR). Rats with a normal birth weight (NBW) or IUGR were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NBW-C and IUGR-C groups) from 6 to 12 weeks. Rats in the IUGR group showed higher levels of glucose and homeostasis model assessment for insulin resistance index (HOMA-IR) (P < 0·05) than in the NBW group. The livers of IUGR rats exhibited higher (P < 0·05) concentration of TAG and lower (P < 0·05) activities of lipolysis enzymes compared with the normal rats. In response to dietary curcumin supplementation, concentrations of serum insulin, glucose and HOMA-IR, pyruvate, TAG, total cholesterol and NEFA in the liver were decreased (P < 0·05). The concentrations of glycogen and activities of lipolysis enzymes in the liver were increased (P < 0·05) in the IUGR-C group compared with the IUGR group. These results were associated with lower (P < 0·05) phosphorylated insulin receptor substrate 1, protein kinase B or Akt, glycogen synthase kinase 3β and expressions of sterol regulatory element binding protein 1 and fatty acid synthase (FASN); decreased expressions for Cd36, sterol regulatory element binding protein 1c (Srebf1) and Fasn; increased (P < 0·05) expression of PPARα; and expressions for Ppara and hormone-sensitive lipase in the liver of IUGR-C rats than the IUGR rats. Maternal malnutrition caused IR and lipid accumulation in the liver. Curcumin supplementation prevented IR by regulating insulin signalling pathways and attenuated hepatic lipid accumulation.

Daytime restricted feeding (2 h of food access from 12.00 to 14.00 hours for 3 weeks) is an experimental protocol that modifies the relationship between metabolic networks and the circadian molecular clock. The precise anatomical locus that controls the biochemical and physiological adaptations to optimise nutrient use is unknown. We explored the changes in liver oxidative lipid handling, such as β-oxidation and its regulation, as well as adaptations in the lipoprotein profile. It was found that daytime restricted feeding promoted an elevation of circulating ketone bodies before mealtime, an altered hepatic daily rhythmicity of 14CO2 production from radioactive palmitic acid, and an up-regulation of the fatty acid oxidation activators, the α-subunit of AMP-activated protein kinase (AMPK), the deacetylase silent mating type information regulation homolog 1, and the transcriptional factor PPARγ-1α coactivator. An increased localisation of phosphorylated α-subunit of AMPK in the periportal hepatocytes was also observed. Liver hepatic lipase C, important for lipoprotein transformation, showed a change of daily phase with a peak at the time of food access. In serum, there was an increase of LDL, which was responsible for a net elevation of circulating cholesterol. We conclude that our results indicate an enhanced fasting response in the liver during daily synchronisation to food access, which involves altered metabolic and cellular control of fatty acid oxidation as well a significant elevation of serum LDL. These adaptations could be part of the metabolic input that underlies the expression of the food-entrained oscillator.

We have compared lipoprotein metabolism in, and susceptibility to atherosclerosis of, two strains of male Golden Syrian hamster, the Bio F1B hybrid and the dominant spot normal inbred (DSNI) strain. When fed a normal low-fat diet containing approximately 40 g fat and 0·3 g cholestero/g, triacylglycerol-rich lipoprotein (chylomicron+VLDL) and HDL-cholesterol were significantly higher (P<0·001) in Bio F1B hamsters than DSNI hamsters. When this diet was supplemented with 150 g coconut oil and either 0·5 or 5·0 g cholestero/g, significant differences were seen in response. In particular, the high-cholesterol diet produced significantly greater increases in plasma cholesterol and triacylglycerol in the Bio F1B compared with the DSNI animals (P=0·002 and P<0·001 for cholesterol and triacylglycerol, respectively). This was particularly dramatic in non-fasting animals, suggesting an accumulation of chylomicrons. In a second experiment, animals were fed 150 g coconut oi/g and 5·0 g cholestero/g for 6 and 12 months. Again, the Bio F1B animals showed dramatic increases in plasma cholesterol and triacylglycerol, and this was confirmed as primarily due to a rise in chylomicron concentration. Post-heparin lipoprotein lipase activity was significantly reduced (P<0·001) in the Bio F1B compared with the DSNI animals at 6 months, and virtually absent at 12 months. Bio F1B animals were also shown to develop significantly more (P<0·001) atherosclerosis. These results indicate that, in the Bio F1B hybrid hamster, cholesterol feeding reduces lipoprotein lipase activity, thereby causing the accumulation of chylomicrons that may be associated with their increased susceptibility to atherosclerosis.

The hypothesis that hepatic lipase mediates the differential hepatic uptake of chylomicron remnants of different fatty acid composition, demonstrated in previous work from our laboratory, was tested by investigating the effect of antibodies to the enzyme on the uptake of remnants enriched with saturated or n-3 polyunsaturated fatty acids by the perfused rat liver. After perfusion of rat livers with polyclonal antibodies to rat hepatic lipase raised in rabbits or with rabbit non-immune serum for 15 min, [3H]oleate-labelled chylomicron remnants, derived from chylomicrons of rats given a bolus of either palm (rich in saturated fatty acids) oil or fish (rich in n-3 polyunsaturated fatty acids) oil, were added. The disappearance of radioactivity from the perfusate during 120 min and its recovery in the liver at the end of the experiments were then measured. Although the rabbit anti-rat hepatic lipase antiserum was shown to inhibit hepatic lipase activity by up to 90 %, and to bind extensively to hepatic sinusoidal surfaces when added to the perfusate, radioactivity from remnants of chylomicrons from rats given a bolus of fish oil as compared with palm oil disappeared from the perfusate and appeared in the liver more rapidly in the presence both the antiserum and the non-immune serum, and the differences between the uptake of the two types of remnants were similar. We conclude, therefore, that differential interaction with hepatic lipase is not responsible for the differences in the rate of removal of chylomicron remnants of different fatty acid composition from the blood.